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目的：探讨细胞因子对人白血病细胞系Ｋ５６２／Ｓ及其多药耐药细胞系Ｋ５６２／Ａ０２的影响。方法：以ＭＴＴ法测定小剂量细胞因子作用后柔红霉素（ＤＮＲ）的毒性变化；用荧光法测定细胞内药物浓度；用免疫组化法检测ｐ－膜糖蛋白（ｐ－ｇｐ）变化；用ＲＴ－ＰＣＲ法检测多药耐药基因（ｍｄｒ－１）ｍＲＮＡ。结果：发现ＤＮＲ对Ｋ５６２／Ａ０２及Ｋ５６２／Ｓ的半数抑制率（ＩＣ５０）分别为４５．０８μｇ／ｍｌ及０．６０７μｇ／ｍｌ。α干扰素（ＩＦＮ－α）和白细胞介素２（ＩＬ－２）作用２４小时可增加ＤＮＲ对Ｋ５６２／Ａ０２的细胞毒作用，与未加药组相比ＩＣ５０下降为１６．３９及１１．９６μｇ／ｍｌ，但不影响Ｋ５６２／Ｓ细胞（ＩＣ５０无明显改变）。且ＩＦＮ－α、ＩＬ－２可提高细胞内ＤＮＲ浓度，从未加药组的２１５１ｎｇ／ｍｇ蛋白到２５７０及２５０３ｎｇ／ｍｇ蛋白。但ｐ－ｇｐ及ｍｄｒ－１ｍＲＮＡ无明显改变。结论：ＩＦＮ－α、ＩＬ－２可增加ＤＮＲ对Ｋ５６２／Ａ０２细胞的毒性作用，增加Ｋ５６２／Ａ０２细胞内的药物浓度，但不是通过下调ｍｄｒ－１ｍＲＮＡ机制而起逆转作用。
Objective: To investigate the effect of cytokines on human leukemia cell line K562/S and its multidrug resistant cell line K562/A02. Methods: The toxicity of daunorubicin (DNR) after low-dose cytokines was measured by MTT assay. The intracellular drug concentration was measured by fluorescence method. The change of p-glycoprotein (p-gp) was detected by immunohistochemistry. The multidrug resistance gene (mdr-1) mRNA was detected by RT-PCR. Results: The IC50 values of DNR on K562/A02 and K562/S were 45.08 μg/ml and 0.607 μg/ml, respectively. Interferon-alpha (IFN-α) and interleukin-2 (IL-2) could increase the cytotoxicity of DNR to K562/A02 for 24 hours, and the IC50 decreased to 16.39 and 11.96 μg compared with the untreated group. /ml, but does not affect K562/S cells (IC50 no significant change). And IFN-α, IL-2 can increase the intracellular DNR concentration, from 2151ng/mg protein to 2570 and 2503ng/mg protein in the non-dosing group. However, there was no significant change in p-gp and mdr-1 mRNA. Conclusion: IFN-α and IL-2 can increase the toxic effect of DNR on K562/A02 cells and increase the drug concentration in K562/A02 cells, but it does not reverse the mechanism of down-regulating mdr-1 mRNA.